arXiv subjects

Tom Britton

Publications and source records attributed to Tom Britton.

At least 19 recordsLinked to original sources

arXiv2026

Bounds on $R_0$ and final epidemic size when the next-generation matrix $M$ is only partially known

We study a multitype SIR epidemic model where individuals are categorized into different types, and where infection spread is characterized by a next-generation matrix $M=\{m_{ij}\}$ with community fractions $\{\pi_j\}$ for the different types of individuals. We analyse two key quantities: the basic reproduction number $R_0$ and the final epidemic outcome of the different types $\{\tau_i\}$. We consider the situation where $M$ is only partly known, through the row sums $\{r_i\}$ or the column sums $\{c_j\}$, and treat both a general $M$ and the special but common situation where $M$ is proportional to a contact matrix satisfying detailed balance. For a general $M$, which is partially observed through $\{r_i\}$ or $\{c_j\}$, we obtain sharp upper and lower bounds of $R_0$ and $\{\tau_i\}$, but for the case where $M$ satisfies detailed balance the problem is harder: our obtained bounds for $R_0$ are narrower than the general case but still not sharp, and bounds for the final size are only obtained when there are two types of individual.

q-bio.PE↗

arXiv2025

Identifiability in epidemic models with prior immunity and under-reporting

Identifiability is the property in mathematical modelling that determines if model parameters can be uniquely estimated from data. For infectious disease models, failure to ensure identifiability can lead to misleading parameter estimates and unreliable policy recommendations. We examine the identifiability of a modified SIR model that accounts for under-reporting and pre-existing immunity in the population. We provide a mathematical proof of the unidentifiability of jointly estimating three parameters: the fraction under-reporting, the proportion of the population with prior immunity, and the community transmission rate, when only reported case data are available. We then show, analytically and with a simulation study, that the identifiability of all three parameters is achieved if the reported incidence is complemented with sample survey data of prior immunity or prevalence during the outbreak. Our results show the limitations of parameter inference in partially observed epidemics and the importance of identifiability analysis when developing and applying models for public health decision making.

stat.ME↗

arXiv2025

Household epidemic models revisited

We analyse a generalized stochastic household epidemic model defined by a bivariate random variable $(X_G, X_L)$, representing the number of global and local infectious contacts that an infectious individual makes during their infectious period. Each global contact is selected uniformly among all individuals and each local contact is selected uniformly among all other household members. The main focus is when all households have the same size $h \geq 2$, and the number of households is large. Large population properties of the model are derived including a central limit theorem for the final size of a major epidemic, the proof of which utilises an enhanced embedding argument. A modification of the epidemic model is considered where local contacts are replaced by global contacts independently with probability $p$. We then prove monotonicity results for the probability of the major outbreak and the limiting final fraction infected $z$ (conditioned on a major outbreak). a) The probability of a major outbreak is shown to be increasing in both $h$ and $p$ for any distribution of $X_L$. b) The final size $z$ increases monotonically with both $h$ and $p$ if the probability generating function (pgf) of $X_L$ is log-convex, which is satisfied by traditional household epidemic models where $X_L$ has a mixed-Poisson distribution. Additionally, we provide counter examples to b) when the pgf of $X_L$ is not log-convex.

math.PR↗

arXiv2025

A multi-season epidemic model with random genetic drift and transmissibility

We consider a model for an influenza-like disease, in which, between seasons, the virus makes a random genetic drift $\delta$, (reducing immunity by the factor $\delta$) and obtains a new random transmissibility $\tau$ (closely related to $R_0$). Given the immunity status at the start of season $k$: $\textbf{p}^{(k)}$, describing community distribution of years since last infection, and their associated immunity levels $\boldsymbol{\iota}^{(k)}$, the outcome of the epidemic season $k$, characterized by the effective reproduction number $R_e^{(k)}$ and the fractions infected in the different immunity groups $\textbf{z}^{(k)}$, is determined by the random pair $(\delta_k, \tau_k)$. It is shown that the immunity status $(\textbf{p}^{(k)}, \boldsymbol{\iota}^{(k)})$, is an ergodic Markov chain, which converges to a stationary distribution $\bar \pi (\cdot) $. More analytical progress is made for the case where immunity only lasts for one season. We then characterize the stationary distribution of $p_1^{(k)}$, being identical to $z^{(k-1)}$. Further, we also characterize the stationary distribution of $(R_e^{(k)}, z^{(k)})$, and the conditional distribution of $z^{(k)}$ given $R_e^{(k)}$. The effective reproduction number $R_e^{(k)}$ is closely related to the initial exponential growth rate $\rho^{(k)}$ of the outbreak, a quantity which can be estimated early in the epidemic season. As a consequence, this conditional distribution may be used for predicting the final size of the epidemic based on its initial growth and immunity status.

math.PR↗

arXiv2024

An epidemic model on a network having two group structures with tunable overlap

A network epidemic model is studied. The underlying social network has two different types of group structures, households and workplaces, such that each individual belongs to exactly one household and one workplace. The random network is constructed such that a parameter $\theta$ controls the degree of overlap between the two group structures: $\theta=0$ corresponding to all household members belonging to the same workplace and $\theta=1$ to all household members belonging to distinct workplaces. On the network a stochastic SIR epidemic is defined, having an arbitrary but specified infectious period distribution, with global (community), household and workplace infectious contacts. The stochastic epidemic model is analysed as the population size $n\to\infty$ with the (asymptotic) probability, and size, of a major outbreak obtained. These results are proved in greater generality than existing results in the literature by allowing for any fixed $0 \leq \theta \leq 1$, a non-constant infectious period distribution, the presence or absence of global infection and potentially (asymptotically) infinite local outbreaks.

math.PR↗

arXiv2024

Improving the use of social contact studies in epidemic modelling

Social contact studies, investigating social contact patterns in a population sample, have been an important contribution for epidemic models to better fit real life epidemics. A contact matrix $M$, having the \emph{mean} number of contacts between individuals of different age groups as its elements, is estimated and used in combination with a multitype epidemic model to produce better data fitting and also giving more appropriate expressions for $R_0$ and other model outcomes. However, $M$ does not capture \emph{variation} in contacts \emph{within} each age group, which is often large in empirical settings. Here such variation within age groups is included in a simple way by dividing each age group into two halves: the socially active and the socially less active. The extended contact matrix, and its associated epidemic model, empirically show that acknowledging variation in social activity within age groups has a substantial impact on modelling outcomes such as $R_0$ and the final fraction $\tau$ getting infected. In fact, the variation in social activity within age groups is often more important for data fitting than the division into different age groups itself. However, a difficulty with heterogeneity in social activity is that social contact studies typically lack information on if mixing with respect to social activity is assortative or not, i.e.\ do socially active tend to mix more with other socially active or more with socially less active? The analyses show that accounting for heterogeneity in social activity improves the analyses irrespective of if such mixing is assortative or not, but the different assumptions gives rather different output. Future social contact studies should hence also try to infer the degree of assortativity of contacts with respect to social activity.

q-bio.PE↗

arXiv2024

An SEIR network epidemic model with manual and digital contact tracing allowing delays

We consider an SEIR epidemic model on a network also allowing random contacts, where recovered individuals could either recover naturally or be diagnosed. Upon diagnosis, manual contact tracing is triggered such that each infected network contact is reported, tested and isolated with some probability and after a random delay. Additionally, digital tracing (based on a tracing app) is triggered if the diagnosed individual is an app-user, and then all of its app-using infectees are immediately notified and isolated. The early phase of the epidemic with manual and/or digital tracing is approximated by different multi-type branching processes, and three respective reproduction numbers are derived. The effectiveness of both contact tracing mechanisms is numerically quantified through the reduction of the reproduction number. This shows that app-using fraction plays an essential role in the overall effectiveness of contact tracing. The relative effectiveness of manual tracing compared to digital tracing increases if: more of the transmission occurs on the network, when the tracing delay is shortened, and when the network degree distribution is heavy-tailed. For realistic values, the combined tracing case can reduce $R_0$ by $20-30\%$, so other preventive measures are needed to reduce the reproduction number down to $1.2-1.4$ for contact tracing to make it successful in avoiding big outbreaks.

physics.soc-ph↗

arXiv2023

SIRS epidemics with individual heterogeneity of immunity waning

We analyse an extended SIRS epidemic model in which immunity at the individual level wanes gradually at exponential rate, but where the waning rate may differ between individuals, for instance as an effect of differences in immune systems. The model also includes vaccination schemes aimed to reach and maintain herd immunity. We consider both the informed situation where the individual waning parameters are known, thus allowing selection of vaccinees being based on both time since last vaccination as well as on the individual waning rate, and the more likely uninformed situation where individual waning parameters are unobserved, thus only allowing vaccination schemes to depend on time since last vaccination. The optimal vaccination policies for both the informed and uniformed heterogeneous situation are derived and compared with the homogeneous waning model (meaning all individuals have the same immunity waning rate), as well as to the classic SIRS model where immunity at the individual level drops from complete immunity to complete susceptibility in one leap. It is shown that the classic SIRS model requires least vaccines, followed by the SIRS with homogeneous gradual waning, followed by the informed situation for the model with heterogeneous gradual waning. The situation requiring most vaccines for herd immunity is the most likely scenario, that immunity wanes gradually with unobserved individual heterogeneity. For parameter values chosen to mimic COVID-19 and assuming perfect initial immunity and cumulative immunity of 12 months, the classic homogeneous SIRS epidemic suggests that vaccinating individuals every 15 months is sufficient to reach and maintain herd immunity, whereas the uninformed case for exponential waning with rate heterogeneity corresponding to a coefficient of variation being 0.5, requires that individuals instead need to be vaccinated every 4.4 months.

q-bio.PE↗

arXiv2022

Epidemic models with digital and manual contact tracing

We analyze a Markovian SIR epidemic model where individuals either recover naturally or are diagnosed, leading to isolation and potential contact tracing. Our focus is on digital contact tracing via a tracing app, considering both its standalone use and combination with manual tracing. We prove that as the population size $n$ grows large, the epidemic process converges to a limiting process, which, unlike typical epidemic models, is not a branching process due to dependencies created by contact tracing. However, by grouping to-be-traced individuals into macro-individuals, we derive a multi-type branching process interpretation, allowing computation of the reproduction number $R$. This is then converted to an individual reproduction number $R^{(ind)}$, which, contrary to $R$, decays monotonically with the fraction of app-users while both share the same threshold at 1. Finally, we compare digital (only) contact tracing and manual (only) contact tracing, proving that the critical fraction app-users $\pi_c$ required for $R=1$ is higher than the critical fraction manually contact traced $p_c$ for manual tracing.

math.PR↗

arXiv2022

Extending SIRS epidemics to allow for gradual waning of immunity

SIRS epidemic models assume that individual immunity (from infection and vaccination) wanes in one big leap, from complete immunity to complete susceptibility. For many diseases immunity on the contrary wanes gradually, something that's become even more evident during COVID-19 pandemic where also recently infected have a reinfection risk, and where booster vaccines are given to increase immunity. This paper considers an epidemic model allowing for such gradual waning of immunity (either linear or exponential waning) thereby extending SIRS epidemics, and also incorporates vaccination. The two versions for gradual waning of immunity are compared with the classic SIRS epidemic, where the three models are calibrated by having the same \emph{average cumulative immunity}. All models are shown to have identical basic reproduction number $R_0$. However, if no prevention is put in place, the exponential waning model has highest prevalence and the classic SIRS model has lowest. Similarly, the amount of vaccine supply needed to reach and maintain herd immunity is highest for the model with exponential decay of immunity and lowest for the classic SIRS model. consequently, if truth lies close to exponential (or linear) decay of immunity, expressions based on the SIRS epidemic will underestimate the endemic level and the critical vaccine supply will not be sufficient to reach and maintain herd immunity. For parameter choices fitting to COVID-19, the critical amount of vaccine supply is about 50% higher if immunity wanes linearly, and more than 150% higher when immunity wanes exponentially, as compared to the classic SIRS epidemic model.

q-bio.PE↗

arXiv2022

Optimal intervention strategies for minimizing total incidence during an epidemic

This article considers the minimization of the total number of infected individuals over the course of an epidemic in which the rate of infectious contacts can be reduced by time-dependent nonpharmaceutical interventions. The societal and economic costs of interventions are taken into account using a linear budget constraint which imposes a trade-off between short-term heavy interventions and long-term light interventions. We search for an optimal intervention strategy in an infinite-dimensional space of controls containing multiple consecutive lockdowns, gradually imposed and lifted restrictions, and various heuristic controls based for example on tracking the effective reproduction number. Mathematical analysis shows that among all such strategies, the global optimum is achieved by a single constant-level lockdown of maximum possible magnitude. Numerical simulations highlight the need of careful timing of such interventions, and illustrate their benefits and disadvantages compared to strategies designed for minimizing peak prevalence. Rather counterintuitively, adding restrictions prior to the start of a well-planned intervention strategy may even increase the total incidence.

math.OC↗

arXiv2022

Nowcasting with leading indicators applied to COVID-19 fatalities in Sweden

The real-time analysis of infectious disease surveillance data, e.g., in the form of a time-series of reported cases or fatalities, is essential in obtaining situational awareness about the current dynamics of an adverse health event such as the COVID-19 pandemic. This real-time analysis is complicated by reporting delays that lead to underreporting of the number of events for the most recent time points (e.g., days or weeks). This can lead to misconceptions by the interpreter, e.g., the media or the public, as was the case with the time-series of reported fatalities during the COVID-19 pandemic in Sweden. Nowcasting methods provide real-time estimates of the complete number of events using the incomplete time-series of currently reported events by using information about the reporting delays from the past. Here, we consider nowcasting the number of COVID-19-related fatalities in Sweden. We propose a flexible Bayesian approach, extending existing nowcasting methods by incorporating regression components to accommodate additional information provided by leading indicators such as time-series of the number of reported cases and ICU admissions. By a retrospective evaluation, we show that the inclusion of ICU admissions as a leading signal improved the nowcasting performance of case fatalities for COVID-19 in Sweden compared to existing methods.

stat.ME↗

arXiv2022

Modelling preventive measures and their effect on generation times in emerging epidemics

We present a stochastic epidemic model to study the effect of various preventive measures, such as uniform reduction of contacts and transmission, vaccination, isolation, screening and contact tracing, on a disease outbreak in a homogeneously mixing community. The model is based on an infectivity process, which we define through stochastic contact and infectiousness processes, so that each individual has an independent infectivity profile. In particular, we monitor variations of the reproduction number and of the distribution of generation times. We show that some interventions, i.e. uniform reduction and vaccination, affect the former while leaving the latter unchanged, whereas other interventions, i.e. isolation, screening and contact tracing, affect both quantities. We provide a theoretical analysis of the variation of these quantities, and we show that, in practice, the variation of the generation time distribution can be significant and that it can cause biases in the estimation of reproduction numbers. The framework, because of its general nature, captures the properties of many infectious diseases, but particular emphasis is on COVID-19, for which numerical results are provided.

q-bio.PE↗

arXiv2021

Analysing the Effect of Test-and-Trace Strategy in an SIR Epidemic Model

Consider a Markovian SIR epidemic model in a homogeneous community. To this model we add a rate at which individuals are tested, and once an infectious individual tests positive it is isolated and each of their contacts are traced and tested independently with some fixed probability. If such a traced individual tests positive it is isolated, and the contact tracing is iterated. This model is analysed using large population approximations, both for the early stage of the epidemic when the "to-be-traced components" of the epidemic behaves like a branching process, and for the main stage of the epidemic where the process of to-be-traced components converges to a deterministic process defined by a system of differential equations. These approximations are used to quantify the effect of testing and of contact tracing on the effective reproduction numbers (for the components as well as for the individuals), the probability of a major outbreak, and the final fraction getting infected. Using numerical illustrations when rates of infection and natural recovery are fixed, it is shown that Test-and-Trace strategy is effective in reducing the reproduction number. Surprisingly, the reproduction number for the branching process of components is not monotonically decreasing in the tracing probability, but the individual reproduction number is conjectured to be monotonic as expected. Further, in the situation where individuals also self-report for testing, the tracing probability is more influential than the screening rate (measured by the fraction infected being screened).

q-bio.PE↗

arXiv2020

The risk for a new COVID-19 wave -- and how it depends on $R_0$, the current immunity level and current restrictions

The COVID-19 pandemic has hit different parts of the world differently: some regions are still in the rise of the first wave, other regions are now facing a decline after a first wave, and yet other regions have started to see a second wave. The current immunity level $\hat i$ in a region is closely related to the cumulative fraction infected, which primarily depends on two factors: a) the initial potential for COVID-19 in the region (often quantified by the basic reproduction number $R_0$), and b) the timing, amount and effectiveness of preventive measures put in place. By means of a mathematical model including heterogeneities owing to age, social activity and susceptibility, and allowing for time-varying preventive measures, the risk for a new epidemic wave and its doubling time, and how they depend on $R_0$, $\hat i$ and the overall effect of the current preventive measures, are investigated. Focus lies on quantifying the minimal overall effect of preventive measures $p_{Min}$ needed to prevent a future outbreak. The first result shows that the current immunity level $\hat i$ plays a more influential roll than when immunity is obtained from vaccination. Secondly, by comparing regions with different $R_0$ and $\hat i$ it is shown that regions with lower $R_0$ and low $\hat i$ may now need higher preventive measures ($p_{Min}$) compared with other regions having higher $R_0$ but also higher $\hat i$, even when such immunity levels are far from herd immunity.

q-bio.PE↗

arXiv2020

Epidemics on networks with preventive rewiring

A stochastic SIR (susceptible $\to$ infective $\to$ recovered) epidemic model defined on a social network is analysed. The underlying social network is described by an Erd\H{o}s-R\'{e}nyi random graph but, during the course of the epidemic, susceptible individuals connected to infectious neighbours may drop or rewire such connections. Large population limits of the model are derived giving both convergence results for the early branching process-like behaviour, and, assuming a major outbreak, the main phase of the epidemic process which converges to a deterministic model that is equivalent to a certain pair approximation model. Law of large numbers results are also obtained for the final size (i.e. total number of individuals infected) of a major outbreak. Two results stand out (valid for a range of parameter set-ups): (i) the limiting final fraction infected may be discontinuous in the infection rate $\lambda$ at its threshold $\lambda_c$ (thus making a discrete jump from $0$ to a strictly positive number) and (ii) for the situation when rewiring is necessarily to uninfected individuals, if it is discontinuous, the limiting final fraction infected jumps from $0$ to $1$ as $\lambda$ passes through $\lambda_c$.

math.PR↗

arXiv2020

Key Questions for Modelling COVID-19 Exit Strategies

Combinations of intense non-pharmaceutical interventions ('lockdowns') were introduced in countries worldwide to reduce SARS-CoV-2 transmission. Many governments have begun to implement lockdown exit strategies that allow restrictions to be relaxed while attempting to control the risk of a surge in cases. Mathematical modelling has played a central role in guiding interventions, but the challenge of designing optimal exit strategies in the face of ongoing transmission is unprecedented. Here, we report discussions from the Isaac Newton Institute 'Models for an exit strategy' workshop (11-15 May 2020). A diverse community of modellers who are providing evidence to governments worldwide were asked to identify the main questions that, if answered, will allow for more accurate predictions of the effects of different exit strategies. Based on these questions, we propose a roadmap to facilitate the development of reliable models to guide exit strategies. The roadmap requires a global collaborative effort from the scientific community and policy-makers, and is made up of three parts: i) improve estimation of key epidemiological parameters; ii) understand sources of heterogeneity in populations; iii) focus on requirements for data collection, particularly in Low-to-Middle-Income countries. This will provide important information for planning exit strategies that balance socio-economic benefits with public health.

q-bio.OT↗

arXiv2020

Summer vacation and COVID-19: effects of metropolitan people going to summer provinces

Many countries are now investigating what the effects of summer vacation might be on the COVID-19 pandemic. Here one particular such question is addressed: what will happen if large numbers of metropolitan people visit a less populated province during the summer vacation? By means of a simple epidemic model, allowing for both short and long-term visitors to the province, it is studied which features are most influential in determining if such summer movements will result in large number of infections among the province population. The method is applied to the island of Gotland off the South East coast of Sweden. It is shown that the amount of mixing between the metropolitan and province groups and the fraction of metropolitan people being infectious upon arrival are most influential. Consequently, minimizing events gathering both the province and metropolitan groups and/or reducing the number of short-term visitors could substantially decrease spreading, as could measures to lower the fraction initially infectious upon arrival.

q-bio.PE↗